Inadvertent lead
placement in the left ventricle (LV) is an uncommon and often
under-diagnosed complication of cardiac device implantation.
Thromboembolic (TE) events are common and usually secondary to fibrosis
or thrombus formation on or around the lead. Anticoagulation can
prevent TE events. Percutaneous and surgical LV lead extractions have
been performed successfully, but the risks of percutaneous lead removal
are not well-defined. In this report, we describe a case of inadvertent
LV lead placement and briefly review the contemporary literature.

Key words: left
ventricular pacing; complication of pacemaker or defibrillator
implantation; lead extraction; left ventricular lead

Case Report

A 78 year-old man with a history of paroxysmal atrial
fibrillation (AF) presented with syncope and underwent implantation of
a dual-chamber Medtronic KDR703 pacemaker while in AF. A Medtronic 4068
ventricular lead was implanted and found to have a threshold of 1.2
Volts (V) at 0.5 ms, a current of 1.8 milliamps and an impedance of 887
ohms. R-wave sensing was noted to be 16.6 mV. A Medtronic 4568 atrial
lead was implanted but threshold testing was not performed and sensing
was not reported. The pacemaker was programmed to VVIR 60-120.

Two months later, the patient developed left upper extremity weakness
and a computed-tomography (CT) scan confirmed the clinical diagnosis of
a right parietal cerebrovascular accident (CVA). The CVA was attributed
to thromboembolism secondary to AF and the patient was initiated on
warfarin therapy with a target INR of 2.0-3.0.

The patient was referred to our clinic after his ventricular lead was
noted to have low impedance and a decrease in sensed R wave amplitude
on routine interrogation. The patient's ECG is shown (Figure 1). The diagnosis of
inappropriate lead placement in the LV was suspected on the basis of
the paced right bundle branch block (RBBB) pattern noted on this ECG.
The diagnosis was confirmed by anterior and lateral chest radiography (Figure 2). A non-contrast chest CT
scan shows the ventricular lead coursing from the right atrium into the
left atrium (LA) through an atrial septum defect (ASD) (Figure 2).

Figure 1. 12-lead
ECG obtained from a patient with an endocardial LV lead with a
RBBB-configuration of the stimulated QRS complex.

Figure 2. A. PA and
lateral chest radiograph from a patient with inadvertent LV lead
placement. The lead in the LV is clearly seen posteriorly on the
lateral view. B. Chest CT from the same patient. The ventricular lead
is seen passing from the RA to the LA through an ASD and from the LA to
the LV through the mitral valve.

Device interrogation revealed a ventricular lead threshold of 1.25 V at
0.4 ms, R wave sensing of 2.8-4.0 mV and a lead impedence of 248 ohms.
The patient was in AF during interrogation with a slow, irregular
ventricular response. No atrial capture could be demonstrated and no P
waves were sensed.

Due to suspected ventricular lead dysfunction and concern that sudden
loss of ventricular pacing would lead to a recurrence of syncope, the
patient underwent lead revision. A St. Jude 1688 lead was inserted into
the right ventricle under fluoroscopic guidance using anterior and
lateral views and the existing atrial lead and LV lead were capped. The
patient's warfarin dose was increased to achieve a target INR of
2.5-3.5. The patient was discharged home without event. At the time of
this report submission, the patient has had no further TE
complications. Given the patient's age and comorbidities, should he
experience further TE complications despite appropriate anticoagulation
or if he develops an absolute contraindication to warfarin, we would
consider percutaneous LV lead extraction with on-site cardiothoracic
surgery back-up.

Discussion

Review

Inadvertent LV pacing due to malpositioned endocardial pacing leads is
a known, but uncommon complication of permanent pacemaker implantation.
A Medline search of English-language articles revealed over 40 cases of
inadvertent LV lead placement. As in our case, passage of the lead
through an ASD or patent foramen ovale was the most common reported
cause of inadvertent LV pacing [1,2]. Inadvertent LV pacing has also
been described in the setting of ventricular septal and apical
perforation [3]. Erroneous cannulation of the subclavian artery and
retrograde passage of the lead into the LV across the aortic valve has
also been reported [4].

TE complications occurred in approximately forty percent of patients
after inadvertent LV lead placement [3,5-7]. Thromboembolism is thought
to have resulted from thrombus formation and fibrosis on or around the
site of lead implantation. Case reports describe syncope, amaurosis
fugax, aphasia and hemiplegia as the most common presenting complaints
of patients with thromboembolism [4,6,8]. TE events have been reported
as soon as one day after lead implantation and up to several years
later [3]. Thromboembolism has been described in several patients
receiving antiplatelet therapy [7]. Other significant complications of
inadvertent LV lead placement included endocarditis, pericardial
effusion, vascular damage and peripheral arterial thrombosis [7].

Time from implantation to diagnosis is highly variable and appears to
influence treatment strategy. Percutaneous LV lead removal has been
successful but only in patients diagnosed less than one year after LV
lead placement [4,9,10]. Fifty percent of patients with and twenty-five
percent of patients without TE complications underwent surgical lead
removal. Inspection of explanted leads showed adherent thrombus in
several cases, including those explanted from asymptomatic patients and
patients receiving aspirin. Notably, transthoracic and transesophageal
echocardiography failed to identify thrombus preoperatively in several
of these cases [7].

Of patients with inadvertent LV lead placement treated without surgery,
only one case of anticoagulation failure with warfarin was reported.
This event occurred in the setting of a subtherapeutic INR (1.6) [3].
Data from 20 patients with intentional endocardial LV lead placement
for cardiac resynchronization indications were also reviewed for TE
complications [11,12]. These data also show a low incidence (one
patient) of thromboembolism with anticoagulation.

Diagnosis

Early activation of the LV during pacing creates a RBBB-pattern on ECG
and, as in our case, is often the key to diagnosis of inadvertent LV
lead placement (Figure 1). This
ECG pattern has good sensitivity but inadequate specificity for LV lead
malposition since a similar pattern may be seen in the setting of RV
dilatation, septal pacing or coronary sinus pacing [13]. Most patients
with malpositioned LV leads, as in our case, have normal pacing
thresholds and this cannot be recommended as a screening tool. As the
patient had normal lead impedances on implantation, we do not
hypothesize that the low impedances noted in our case relate directly
to endocardial LV lead placement. Chest radiography, in contrast, is
often helpful in delineating the position of the ventricular lead and
can therefore be used a confirmatory test in suspected lead malposition
(Figure 2).

It is advisable that all patients undergoing device implantation have a
12-lead ECG recorded during pacing. Consideration should also be given
to routine post-implantation anterior and lateral chest radiography. At
a minimum, those with a RBBB-pattern during pacing should receive both
an anterior and lateral chest radiograph. If lead malposition is
suspected, echocardiography can be helpful in confirming the diagnosis
and determining the course of the lead but, due to its poor sensitivity
in published reports, should not be used to 'rule out' the presence of
thrombus [4,14].

Management

If a diagnosis of inadvertent lead placement in the LV is made
immediately after implant, percutaneous lead extraction can reduce the
risk of future TE events without the need for lifelong anticoagulation.
While percutaneous LV lead extraction has been performed successfully
up to 9 months after implantation, this procedure carries a risk of
systemic embolization from lead manipulation, especially if a laser
sheath is used [9,10]. While thrombus formation has occurred in the
first 24-48 hours after LV lead implantation, percutaneous lead
extraction is appealing in this period because it does not require the
use of a laser sheath and thus may have lower procedural risk than
surgical lead removal with use of cardiopulmonary bypass.

For those patients in whom the diagnosis of inadvertent LV lead
placement is delayed, anticoagulation with warfarin is reasonable as no
TE events have been reported in patients with an INR of 2.5-3.5 [12].
Use of antiplatelet therapy as a sole means of TE prophylaxis in
patients with inadvertent LV lead placement is not advisable. Surgical
LV lead extraction also warrants consideration, especially if cardiac
surgery has to be performed for another indication. Surgical lead
extraction may be preferable in younger patients in whom the risk of
surgery is lower and the planned duration of warfarin longer.

Conclusions

While uncommon, inadvertent LV lead placement is a potentially
devastating complication of pacemaker implantation. Appropriate
analysis of the paced QRS pattern on ECG and post-implantation chest
radiograph may reduce morbidity and mortality by promoting early
recognition and treatment. Percutaneous lead extraction is an option
for patients diagnosed in the immediate post-operative period. Surgical
lead removal or lifelong anticoagulation should be considered for
patients in whom the diagnosis of inadvertent LV lead placement is
delayed.